Mutation of Dcdc2 in mice leads to impairments in auditory processing and memory ability
Dyslexia is a complex neurodevelopmental disorder characterized by impaired reading ability despite normal intellect, and is associated with specific difficulties in phonological and rapid auditory processing (RAP), visual attention and working memory. Genetic variants in Doublecortin domain‐contain...
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Published in | Genes, brain and behavior Vol. 13; no. 8; pp. 802 - 811 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
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Oxford, UK
Blackwell Publishing Ltd
01.11.2014
John Wiley & Sons, Inc |
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Abstract | Dyslexia is a complex neurodevelopmental disorder characterized by impaired reading ability despite normal intellect, and is associated with specific difficulties in phonological and rapid auditory processing (RAP), visual attention and working memory. Genetic variants in Doublecortin domain‐containing protein 2 (DCDC2) have been associated with dyslexia, impairments in phonological processing and in short‐term/working memory. The purpose of this study was to determine whether sensory and behavioral impairments can result directly from mutation of the Dcdc2 gene in mice. Several behavioral tasks, including a modified pre‐pulse inhibition paradigm (to examine auditory processing), a 4/8 radial arm maze (to assess/dissociate working vs. reference memory) and rotarod (to examine sensorimotor ability and motor learning), were used to assess the effects of Dcdc2 mutation. Behavioral results revealed deficits in RAP, working memory and reference memory in Dcdc2del2/del2 mice when compared with matched wild types. Current findings parallel clinical research linking genetic variants of DCDC2 with specific impairments of phonological processing and memory ability.
Dcdc2 mutant mice show impaired working and reference memory performance on a 4/8 radial arm water maze. |
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AbstractList | Dyslexia is a complex neurodevelopmental disorder characterized by impaired reading ability despite normal intellect, and is associated with specific difficulties in phonological and rapid auditory processing (RAP), visual attention and working memory. Genetic variants in Doublecortin domain-containing protein 2 (DCDC2) have been associated with dyslexia, impairments in phonological processing and in short-term/working memory. The purpose of this study was to determine whether sensory and behavioral impairments can result directly from mutation of the Dcdc2 gene in mice. Several behavioral tasks, including a modified pre-pulse inhibition paradigm (to examine auditory processing), a 4/8 radial arm maze (to assess/dissociate working vs. reference memory) and rotarod (to examine sensorimotor ability and motor learning), were used to assess the effects of Dcdc2 mutation. Behavioral results revealed deficits in RAP, working memory and reference memory in Dcdc2del2/del2 mice when compared with matched wild types. Current findings parallel clinical research linking genetic variants of DCDC2 with specific impairments of phonological processing and memory ability. Dyslexia is a complex neurodevelopmental disorder characterized by impaired reading ability despite normal intellect, and is associated with specific difficulties in phonological and rapid auditory processing (RAP), visual attention and working memory. Genetic variants in Doublecortin domain-containing protein 2 (DCDC2) have been associated with dyslexia, impairments in phonological processing and in short-term/working memory. The purpose of this study was to determine whether sensory and behavioral impairments can result directly from mutation of the Dcdc2 gene in mice. Several behavioral tasks, including a modified pre-pulse inhibition paradigm (to examine auditory processing), a 4/8 radial arm maze (to assess/dissociate working vs. reference memory) and rotarod (to examine sensorimotor ability and motor learning), were used to assess the effects of Dcdc2 mutation. Behavioral results revealed deficits in RAP, working memory and reference memory in Dcdc2del2/del2 mice when compared with matched wild types. Current findings parallel clinical research linking genetic variants of DCDC2 with specific impairments of phonological processing and memory ability. Dcdc2 mutant mice show impaired working and reference memory performance on a 4/8 radial arm water maze. Dyslexia is a complex neurodevelopmental disorder characterized by impaired reading ability despite normal intellect, and is associated with specific difficulties in phonological and rapid auditory processing, visual attention, and working memory. Genetic variants in DCDC2 have been associated with dyslexia, impairments in phonological processing, and in short term/working memory. The purpose of this study was to determine whether sensory and behavioral impairments can result directly from mutation of the Dcdc2 gene in mice. Several behavioral tasks, including a modified pre-pulse inhibition paradigm (to examine auditory processing), a 4/8 radial arm maze (to assess/dissociate working versus reference memory), and rotarod (to examine sensorimotor ability and motor learning) were used to assess the effects of Dcdc2 mutation. Behavioral results revealed deficits in rapid auditory processing, working memory, and reference memory in Dcdc2 del2/del2 mice as compared to matched wild types. Current findings parallel clinical research linking genetic variants of DCDC2 with specific impairments of phonological processing and memory ability. Dyslexia is a complex neurodevelopmental disorder characterized by impaired reading ability despite normal intellect, and is associated with specific difficulties in phonological and rapid auditory processing (RAP), visual attention and working memory. Genetic variants in Doublecortin domain‐containing protein 2 ( DCDC2 ) have been associated with dyslexia, impairments in phonological processing and in short‐term/working memory. The purpose of this study was to determine whether sensory and behavioral impairments can result directly from mutation of the Dcdc2 gene in mice. Several behavioral tasks, including a modified pre‐pulse inhibition paradigm (to examine auditory processing), a 4/8 radial arm maze (to assess/dissociate working vs. reference memory) and rotarod (to examine sensorimotor ability and motor learning), were used to assess the effects of Dcdc2 mutation. Behavioral results revealed deficits in RAP, working memory and reference memory in Dcdc2 del2/del2 mice when compared with matched wild types. Current findings parallel clinical research linking genetic variants of DCDC2 with specific impairments of phonological processing and memory ability. Dyslexia is a complex neurodevelopmental disorder characterized by impaired reading ability despite normal intellect, and is associated with specific difficulties in phonological and rapid auditory processing (RAP), visual attention and working memory. Genetic variants in Doublecortin domain‐containing protein 2 (DCDC2) have been associated with dyslexia, impairments in phonological processing and in short‐term/working memory. The purpose of this study was to determine whether sensory and behavioral impairments can result directly from mutation of the Dcdc2 gene in mice. Several behavioral tasks, including a modified pre‐pulse inhibition paradigm (to examine auditory processing), a 4/8 radial arm maze (to assess/dissociate working vs. reference memory) and rotarod (to examine sensorimotor ability and motor learning), were used to assess the effects of Dcdc2 mutation. Behavioral results revealed deficits in RAP, working memory and reference memory in Dcdc2del2/del2 mice when compared with matched wild types. Current findings parallel clinical research linking genetic variants of DCDC2 with specific impairments of phonological processing and memory ability. Dcdc2 mutant mice show impaired working and reference memory performance on a 4/8 radial arm water maze. Dyslexia is a complex neurodevelopmental disorder characterized by impaired reading ability despite normal intellect, and is associated with specific difficulties in phonological and rapid auditory processing (RAP), visual attention and working memory. Genetic variants in Doublecortin domain-containing protein 2 (DCDC2) have been associated with dyslexia, impairments in phonological processing and in short-term/working memory. The purpose of this study was to determine whether sensory and behavioral impairments can result directly from mutation of the Dcdc2 gene in mice. Several behavioral tasks, including a modified pre-pulse inhibition paradigm (to examine auditory processing), a 4/8 radial arm maze (to assess/dissociate working vs. reference memory) and rotarod (to examine sensorimotor ability and motor learning), were used to assess the effects of Dcdc2 mutation. Behavioral results revealed deficits in RAP, working memory and reference memory in Dcdc2(del2/del2) mice when compared with matched wild types. Current findings parallel clinical research linking genetic variants of DCDC2 with specific impairments of phonological processing and memory ability. |
Author | Szalkowski, C. E. Truong, D. T. LoTurco, J. J. Holly Fitch, R. Che, A. Rendall, A. R. Galaburda, A. M. |
AuthorAffiliation | 2 Department of Physiology and Neurobiology, University of Connecticut, 75 North Eagleville Road, Unit 3156, Storrs, CT 06269 3 Department of Neurology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02215 1 Department of Psychology/Behavioral Neuroscience, University of Connecticut, 406 Babbidge Road, Unit 1020, Storrs, CT 06269 |
AuthorAffiliation_xml | – name: 2 Department of Physiology and Neurobiology, University of Connecticut, 75 North Eagleville Road, Unit 3156, Storrs, CT 06269 – name: 1 Department of Psychology/Behavioral Neuroscience, University of Connecticut, 406 Babbidge Road, Unit 1020, Storrs, CT 06269 – name: 3 Department of Neurology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02215 |
Author_xml | – sequence: 1 givenname: D. T. surname: Truong fullname: Truong, D. T. organization: University of Connecticut – sequence: 2 givenname: A. surname: Che fullname: Che, A. organization: University of Connecticut – sequence: 3 givenname: A. R. surname: Rendall fullname: Rendall, A. R. organization: University of Connecticut – sequence: 4 givenname: C. E. surname: Szalkowski fullname: Szalkowski, C. E. organization: University of Connecticut – sequence: 5 givenname: J. J. surname: LoTurco fullname: LoTurco, J. J. organization: University of Connecticut – sequence: 6 givenname: A. M. surname: Galaburda fullname: Galaburda, A. M. organization: Beth Israel Deaconess Medical Center and Harvard Medical School – sequence: 7 givenname: R. surname: Holly Fitch fullname: Holly Fitch, R. organization: University of Connecticut |
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Keywords | Dcdc2 rapid auditory processing working memory language impairment dyslexia |
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Title | Mutation of Dcdc2 in mice leads to impairments in auditory processing and memory ability |
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